Homeostatic plasticity

From Wikipedia, the free encyclopedia
Jump to: navigation, search

In neuroscience, homeostatic plasticity refers to the capacity of neurons to regulate their own excitability relative to network activity,[1][2] a compensatory adjustment that occurs over the timescale of days. Synaptic scaling has been proposed as a potential mechanism of homeostatic plasticity.[3]

Homeostatic plasticity is thought to balance Hebbian plasticity by modulating the activity of the synapse or the properties of ion channels. Homeostatic plasticity in neocortical circuits has been studied in depth by Gina G. Turrigiano and Sacha Nelson of Brandeis University, who first observed compensatory changes in excitatory postsynaptic currents (mEPSCs) after chronic activity manipulations.[4]

Homeostatic plasticity can be used to term a process that maintains the stability of neuronal functions through a coordinated plasticity among subcellular compartments, such as the synapses versus the neurons and the cell bodies versus the axons.[5]

Homeostatic plasticity also maintains neuronal excitability in a real-time manner through the coordinated plasticity of threshold and refractory period at voltage-gated sodium channels.[6]

The term homeostatic plasticity derives from two opposing concepts: 'homeostatic' (a product of the Greek words for 'same' and 'state' or 'condition') and plasticity (or 'change'), thus homeostatic plasticity means "staying the same through change."

References[edit]

  1. ^ Turrigiano, G. G.; Nelson, S. B. (2004). "Homeostatic plasticity in the developing nervous system". Nature Reviews Neuroscience. 5 (2): 97–107. PMID 14735113. doi:10.1038/nrn1327. 
  2. ^ Surmeier, D. J.; Foehring, R. (2004). "A mechanism for homeostatic plasticity". Nature Neuroscience. 7 (7): 691–2. PMID 15220926. doi:10.1038/nn0704-691. 
  3. ^ Turrigiano, G (2012). "Homeostatic synaptic plasticity: Local and global mechanisms for stabilizing neuronal function". Cold Spring Harbor Perspectives in Biology. 4 (1): a005736. PMC 3249629Freely accessible. PMID 22086977. doi:10.1101/cshperspect.a005736. 
  4. ^ Turrigiano, G. G.; Leslie, K. R.; Desai, N. S.; Rutherford, L. C.; Nelson, S. B. (1998). "Activity-dependent scaling of quantal amplitude in neocortical neurons". Nature. 391 (6670): 892–6. PMID 9495341. doi:10.1038/36103. 
  5. ^ Chen, Na; Chen, Xin; Jin-Hui (2008). "Homeostasis by coordination of subcellular compartment plasticity improves spike encoding". Journal of Cell Science. 121 (17): 2961–2971. doi:10.1242/jcs.022368. 
  6. ^ Ge, Rongjing; Chen, Na; Jin-Hui (2009). "Real-time neuronal homeostasis by coordinating VGSC intrinsic properties". Biochemical and Biophysical Research Communications. 387: 585–589. PMID 19616515. doi:10.1016/j.bbrc.2009.07.066. 

External links[edit]